Additional file 1 of Clec7a drives gut fungus-mediated host lipid deposition

Additional file 1: Supplemental Fig. 1. Differences in gut fungi in obese animal models. (A) Fungal diversity between obese Shaziling (SZL) pigs and lean Yorkshire pigs (n=5); (B) Fungal diversity between obese Ningxiang (NX) pigs and lean DLY pigs (n=7 or 8); (C) Fungal diversity in HFD fed mice (n=7); (D) Fungal phyla and makers (genus) in obese Shaziling (SZL) pigs (n=5); (E) Fungal phyla and makers (genus) in Ningxiang (NX) pigs (n=7 or 8); (F) Fungal phyla and makers (genus) in HFD fed mice (n=5). Differences among the groups were compared using Student’s t test. *p<0.05; ***p<0.001. Supplemental Fig. 2. Fungi deficiency protects mice against diet-induced obesity. (A-F) Body weight (A), final body weight (B), the relative weight of SAT (C), AAT (D), PEAT (E), and white adipose tissue enlargement in fluconazole (Flu) treated male mice. 7 weeks old-male C57BL/6 mice were treated with fluconazole (Flu) for 16 weeks (n=8); (G, H) Western blot of dectin1 expression (n=3); (I-M) Body weight (I), the relative weight of SAT (J), total white adipose tissue (TWAT) (K), serum TC (L), and HDL (M) in fluconazole (Flu) treated female mice (n=10). 6-7 weeks old-female C57BL/6 mice were treated with fluconazole (Flu) lasted for 16 weeks to test the role of gut fungi in different sexes (n=8-10). Differences among the groups were compared using Student’s t test. *p<0.05; **p<0.01; ***p<0.001; ns p>0.05. Supplemental Fig. 3. Fecal microbial compositions in FMT and cohoused mice. (A-D) α-diversity (A) and β-diversity (B) of gut fungi in cohoused with control mice, α-diversity (C) and β-diversity (D) of gut fungi in cohoused with obese mice (n=6); (E-H) α-diversity (E) and β-diversity (F) of gut fungi in cohoused with with obese mice, α-diversity (G) and β-diversity (H) of gut bacteria in FMT mice (n=8). Differences among the groups were compared using Student’s t test. *p<0.05; **p<0.01; ***p<0.001; ns p>0.05. Supplemental Fig. 4. Fungal communities are associated with the host obese phenotype. (A) 10 differentiated genres from Fig.3C between obese and lean mice; (B-D) Serum TC (B), LDL (C), and liver lipid in fungus treated HFD mice (n=14 or 16). HFD mice (7 week old, male, C57BL/6) were colonized with fungus Ascomycota_sp (Asco) and Microascaceae_sp (Micro) for 14 weeks to test the role of fat weight-related fungi in HFD-induced obesity (n=13-16). The liver lipid was stained with oil O and the redder indicated more lipid depositions; (E) Glucose metabolism gene expression with fungus supplementation (n=8); (F-O) Body weight (F), final body weight (G), the relative weight of SAT (H) and PEAT(II), serum TC (J) and LDL (K), and adipocyte area of SAT and PEAT (L-O) of fungus treated obese mice. Obese mice (male, C57BL/6, 39.1±0.1g ) were induced by feeding HFD for 20 weeks (fat), then replaced by the standard chow and challenged with two fungi for 14 weeks (n=9-10). Differences among the groups were compared using Student’s t test. *p<0.05; **p<0.01; ***p<0.001; ns p>0.05. Supplemental Fig. 5. Fecal bacterial composition in fungi-deficient mice. (A) Fecal DNA of bacteria and fungi with RT-PCR in fungi-deficient mice (n=8); (B-F) a-diversity (B), β-diversity (C), top 10 phyla (D), Firmicutes/Bacteroidetes ratio (E),top 30 genre (F) in fungi-deficient mice. Fecal bacterial compositions of HFD (feeding 12 weeks) and fluconazole (Flu) treated mice were sequenced by 16S rDNA (n=12-13). Differences among the groups were compared using Student’s t test. *p<0.05; **p<0.01; ***p<0.001; ns p>0.05. Supplemental Fig. 6. Dectin-1 expression in obese mice. (A) Western blot in Lean and Obese mice fed HFD (n=3); (B) Western blot in HFD fed mice (n=3). Differences among the groups were compared using Student’s t test. *p<0.05; **p<0.01; ***p<0.001; ns p>0.05.